Mucin dynamics in intestinal bacterial infection

Sara K Lindén1, Timothy H J Florin, Michael A McGuckin

  • 1Mucosal Diseases Program, Mater Medical Research Institute, Mater Health Services, South Brisbane, Queensland, Australia.

Plos One
|December 18, 2008
PubMed
Abstract

Insights

Intestinal mucins, like Muc2, limit bacterial access. During infection, cell-surface mucin Muc1 increases, while others decrease, indicating major changes in the gut barrier response.

Area of Science:

  • Microbiology
  • Immunology
  • Gastroenterology

Background:

  • Bacterial gastroenteritis is a significant global health issue.
  • Citrobacter rodentium infection in mice serves as a model for human enteropathogenic E. coli.
  • Mucin glycoproteins form the primary physical barrier in the intestinal tract.

Purpose of the Study:

  • To investigate the expression of various mucins in the mouse intestine during Citrobacter rodentium infection.
  • To understand the role of mucins in host defense against bacterial gastroenteritis.

Main Methods:

  • Immunohistochemistry was used to analyze mucin expression (Alcian blue/PAS, Muc1, Muc2, Muc4, Muc5AC, Muc13, Muc3/17) in healthy and infected mice.
  • In vitro binding assays were performed to assess the interaction between C. rodentium and Muc2.
  • Bacterial load and localization were examined in vivo.

Main Results:

  • C. rodentium infection led to colitis and systemic infection in mice by day 12.
  • C. rodentium bound to Muc2 in vitro, and bacteria were found within secreted Muc2 in vivo, suggesting mucins limit epithelial access.
  • While most mucins remained unchanged in the small intestine, cecum, and proximal colon, distal colonic epithelium showed decreased secreted and cell-surface mucins, except for an increase in Muc1.
  • Human infections (Salmonella St Paul, Campylobacter jejuni, Clostridium difficile) also induced MUC1 in the colon.

Conclusions:

  • Intestinal infection triggers significant alterations in both cell-surface and secreted mucins.
  • Mucins play a crucial role in the host's innate immune response to bacterial gastroenteritis.

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